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The Journal of Venomous Animals and Toxins including Tropical Diseases

ISSN 1678-9199 | 2010 | volume 16 | issue 3 | pages 519-523

Unusual visual loss after snakebite


C ase R epor t

Tungpakorn N (1)

(1) Department of Ophthalmology, Sawanpracharak Hospital, Nakhonsawan, Thailand.

Abstract: Snakebites are endemic in some parts of Thailand, being associated with several complications.
Ocular disturbances are uncommon, except in cases of corneal or conjunctival injury, when the eye is
directly exposed to the snake venom. The present study presents a case of combined ophthalmic artery
occlusion and transient central retinal artery occlusion with macular ischemia after a Russell’s viper bite.

Key words: snakebite, central retinal artery occlusion, macular ischemia, Vipera russelli siamensis.

INTRODUCTION CASE REPORT

Snakebites are a common medical emergency A 32-year-old Thai man was bitten by a snake
in the tropics, particularly in rural and farming on his right foot while working in a sugarcane
areas. Venomous snakebites may result in field. The snake (Russell’s viper, subspecies Vipera
neurologic or hemostatic dysfunction, and cause russelli siamensis) threatened, bit and escaped
multisystemic involvement. Viperidae venoms but the species was confirmed by the patient
act mainly on blood and blood vessels. Reports and witnesses. He slowly lost consciousness for
of ophthalmic manifestations after viperine three hours after the bite. He was admitted to
snakebites include subconjunctival hemorrhage, a local general hospital in an unconscious state
hyphema, retinal hemorrhage, vitreous and received first aid, including prompt medical
hemorrhage, central retinal artery occlusion, treatment and supportive care. Russell’s viper anti-
visual loss due to cortical infarction, and macular snake venom (ASV) was given due to prolonged
infarction (1-5). venous clotting time (VCT > 30 minutes). He was
Ophthalmic artery occlusion, retinal necrosis, transferred immediately to the medical intensive
and macular infarction associated with snakebites care unit at the Sawanpracharak Hospital,
are infrequent ocular effects, and to the best of our Nakhonsawan, Thailand.
knowledge only one case has been reported in the At the time of admission, he was drowsy, with
literature (5). This paper reports the development a Glasgow Coma Score (GCS) of 9 (E2V2M5),
of secondary ophthalmic artery occlusion and his pulse was 120 beats per minute, blood
transient central retinal artery occlusion with pressure 110/60 mmHg, and presented normal
macular ischemia after viper envenomation in a respirations. Fang marks were visible on the right
single case study. foot with a minimal localized swelling. Bleeding
Tungpakorn N. Unusual visual loss after snakebite

from the bite site was observed. Blood laboratory eye. His best corrected visual acuity (BCVA)
tests revealed normal hemoglobin level (13.0 g/ was recorded as 6/6 in the right eye (OD) and
dL), normal platelet count (137,000 cells/µL), no light perception in the left eye (OS). The
decreased fibrinogen (143 mg/dL; normal = intraocular pressures were 12 mmHg OD and
248-328 mg/dL), prolonged prothrombin time 10 mmHg OS. Ocular examination disclosed
(> 200 seconds; normal = 12.0-16.5 seconds) unremarkable anterior segment in both his eyes.
and prolonged partial prothrombin time (> 200 Relative afferent pupillary defect was observed
seconds; normal = 25.0-40.0 seconds) while VCT in the left eye. Fundus examination revealed
returned to 18 minutes. Results of renal function diffuse whitening and swollen mark of the entire
tests, electrocardiography, and computed retina and choroid, possibly by decreasing mark
tomography of the brain were normal. of both retinal and choroidal perfusion. By
The patient regained consciousness 18 hours increasing contrast to the white background, the
after the snakebite. Five hours later, he noticed left optic disc color and macula appeared more
and started complaining of diminished vision reddish (Figure 1). Unfortunately, there was no
in his left eye. He sought an ophthalmology fluorescein angiography reported due to lack of
consultation a couple of days after the snakebite information regarding the status of choroidal
due to a rapid painless visual loss in his left circulation during the first visit.

Figure 1. Fundus photograph showing marked whitish retina and a cherry-red spot at the macula of the
left eye.

Figure 2. Fundus photograph showing the outer retinal ischemia minimally subsided, as seen by decreased
swelling and reddish fundus, and still perifoveal whitening of the inner retina in the left eye.

J Venom Anim Toxins incl Trop Dis | 2010 | volume 16 | issue 3 520
Tungpakorn N. Unusual visual loss after snakebite

Figure 3. Fundus photograph and fluorescein angiography of the left eye showed resolutions of retinal
whitening, generalized attenuation of retinal vessels especially inferotemporal branch, and atrophic
macula with clumping pigment. Optic disc appeared slightly pale and atrophic.

Two weeks later, the choroidal background DISCUSSION


appeared more reddish than previously observed
and the fundus picture presented more whitening Snake venom is a complex mixture of several
of the macula which may be interpreted by the enzymes and proteins, toxic polypeptides, and
increased contrast by reperfusion of the choroidal inorganic components. It contains numerous
system. Also, the macula became more swollen, toxins, and their combined action has a more
confirmed by +78 D contact lens examination potent effect than that of their individual
(Figure 2). effects. In general, venoms are described as
Six weeks after the incident, fundoscopic either neurotoxic or hematotoxic. Systemic
examination in the left eye showed large cupping, manifestations of snakebites depend on
atrophic and pale optic disc. All the major retinal specific toxins that constitute the venom. Also,
arterioles showed attenuation, especially on the Viperidae snake venom is comprised of mixed
inferotemporal branch, which were confirmed by enzymes and toxins with rich components
the angiogram. There were some coarse granular dominantly affecting hemostatic mechanisms,
changes of the pigmented background. The foveal some of which appear to have opposing
avascular zone was enlarged and all the arterioles effects (6). While there are enzymes that cause
around it ended abruptly (Figure 3). Ocular hypofibrinogenemia, hypoprothrombinemia,
treatment was ineffective since the patient was not thrombocytopenia and fibrinolysis; at the same
responsive to standard treatments. In addition, the time, there are potent proteases (e.g. arginine
visual prognosis was extremely poor in his left eye. esterase and hydrolase) acting as activators of

J Venom Anim Toxins incl Trop Dis | 2010 | volume 16 | issue 3 521
Tungpakorn N. Unusual visual loss after snakebite

coagulation factors X and V, thereby promoting • Finally, the direct action of the venom toxins
coagulation (7). In addition, enzymes – such or fibrin emboli into the ophthalmic artery
as hyaluronidase – damage connective tissues, which later result in retinal arteriolar ischemia
leading to enhanced toxin dissemination. The and choroidal ischemia (12).
net effect of these enzymes is activation of the
intrinsic coagulation pathway, leading to the Ocular complications resulting from snakebite
formation of numerous microthrombi in the are not commonly reported in the literature.
circulation and, therefore, consumption of However, subconjunctival hemorrhage,
coagulation factors and platelets (8, 9). The end hyphema, retinal and vitreous hemorrhages
result is usually internal and external bleeding are well-known effects of viper envenomation.
due to disseminated intravascular coagulation Other rare problems described included ptosis,
(DIC) that may cause massive intravascular ophthalmoplegia, keratomalacia, uveitis, central
coagulation with consequent ischemic sequel retinal artery occlusion, unilateral or bilateral
to major organs (10). Toxic vasculitis caused by optic neuritis, visual loss due to cortical infarction,
certain viperine species may result in thrombosis and macular infarction (3-5, 15).
or indicate direct action of the venom on vascular In conclusion, the patient had an ophthalmic
endothelial cells (11, 12). artery occlusion and transient central retinal
Lastly, hemorrhagins – complement-mediated occlusion with secondary macular infarction
toxic components of Viperidae snake venom – after the snakebite. Although it is rare, it can
may provoke severe vascular spasm, endothelial become very severe and lead to vision-threatening
damage, and increased vascular permeability, all situations. However, the actual cause of this case
of which might contribute to vascular occlusion has not been reported or literately confirmed.
(11, 12). Moreover, hyperviscosity caused by
hypovolemia and hypoperfusion secondary ACKNOWLEDGEMENTS
to hypotension may also contribute to vessel Special thanks for all physicians at
occlusion. Any inherent deficiency of protein Sawanpracharak Hospital, Nakhonsawan, who
C, protein S, and antithrombin III may manifest participated in treating this patient.
too (13).
Various mechanisms that have been proposed COPYRIGHT
as causative of rare complication after snake bite © CEVAP 2010
in this case are summarized below:
• Disseminated intravascular coagulopathy SUBMISSION STATUS
induced by the viper toxins may cause Received: January 13, 2010.
vessel-occlusive thrombi (especially with an Accepted: May 19, 2010.
underlying procoagulant state), which can Abstract published online: June 7, 2010.
account for the thrombi in the ophthalmic Full paper published online: August 31, 2010.
artery (11).
• Variations in viper venom composition, in CONFLICTS OF INTEREST
terms of its hemorrhagic, anticoagulant, and There is no conflict.
other activities, may favor thrombosis, as
opposed to bleeding (14). CORRESPONDENCE TO
• Snake venom hemorrhagins could be NARONG TUNGPAKORN, Department of
responsible for inducing vasculitis, which Ophthalmology, Sawanpracharak Hospital,
leads to vasospasm, endothelial damage and Nakhonsawan, Thailand, 60000. Phone: +66 0
increased vascular permeability (12). 5621 9888. Fax: +66 0 5621 9899. Email: mootpk@
• A preexisting procoagulant state, due to a yahoo.com.
mutation in factor V, deficiencies of protein
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